Carbon Monoxide

  • Small increase in CO partial pressure leads to large increase in COHb. 
  • When this occurs hemoglobin and O2 partial pressure may be normal = false normal readings of SpO2
  • CO also interacts with other small gaseous ligands (free radical nitric oxide).
    • Accumulation of free radical NO leads to:
      • Activation of NMDA
      • Release of NE and AA
      • Endothelial injury
      • Neutrophil activation
      • Lipid peroxidation
  • CO binds to Cytochrome C oxidase => inhibiting ATP synthesis, generation of hydroxyl radicals
  • Prolonged exposure to CO => “soaking” = capillary leakage, inflammatory molecules -> pulmonary edema = Not observed in acute exposure
  • Delayed neurologic injury: most frequent form of CO morbidity: impairments in concentration, learning, dementia, cogwheel rigidity, amnesia, depression.
  • Nitrotyrosine, major product when peroxynitrite reacts with proteins can be measured and elevated when exposed to CO for > 40 min.

For more chapters, visit the ABAT Study Guide homepage

Carbon Monoxide

Carbon Monoxide

Small increase in CO partial pressure leads to large increase in COHb. When this occurs hemoglobin and O2 partial pressure may be normal = false normal readings of SpO2CO also interacts with other small gaseous ligands (free radical nitric oxide).Accumulation of free radical NO leads to:Activation of NMDARelease of NE and AAEndothelial injuryNeutrophil activationLipid peroxidationCO binds to Cytochrome C oxidase => inhibiting ATP synthesis, generation of ydroxyl radicalsProlonged exposure to CO => “soaking” = capillary leakage, inflammatory molecules -> pulmonary edema = Not observed in acute exposureDelayed neurologic injury: most frequent form of CO morbidity: impairments in concentration, learning, dementia, cogwheel rigidity, amnesia, depression.Nitrotyrosine, major product when peroxynitrite reacts with proteins can be measured and elevated when exposed to CO for > 40 min.For more chapters, visit the ABAT Study Guide homepageCarbon Monoxide